In contrast, TP53, GATA2, KRAS, RUNX1, STAG2, ASXL1, ZRS2 and TET2 mutations are enriched in high-risk MDS compared to low-risk MDS and had a weaker impact, compared to the other mutations, on sAML progression [37]. This evidence concerns the gene ASXL1 and myelodysplastic syndrome.